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MOTS-c Peptide Introduction and Overview
MOTS-c Mitochondrial Peptide – 20 mg (Research Grade)
€180,00
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MOTS-c Peptide Introduction and Overview
This research-grade peptide is supplied exclusively for laboratory and experimental use. MOTS-C is examined in experimental models investigating mitochondrial signaling, cellular energy regulation, and metabolic adaptation. Research interest centers on how cells respond to energetic stress and efficiency-related signals.
MOTS-c (Mitochondrial Open Reading Frame of the 12S rRNA Type-c) is a 16-amino acid peptide encoded by the mitochondrial genome (mtDNA). Discovered in 2015, it functions as a mitochondrial-derived peptide (MDP) with systemic regulatory roles. Unlike traditional mitochondrial proteins, MOTS-c translocates from mitochondria to the nucleus, influencing gene expression and metabolic pathways. Its molecular-level mechanism of action (MoA) centers on modulating cellular energy homeostasis, primarily through AMPK activation and purine metabolism interference. Recent studies (2025-2026) highlight its potential in metabolic disorders, aging, and neurodegeneration, with applications as an exercise mimetic. Structurally distinct from other MDPs like Humanin (a 24-amino acid peptide), MOTS-c shares cytoprotective effects but targets different pathways, making it promising for neurodegenerative diseases such as Alzheimer's and Parkinson's.
Core Molecular Mechanism
At the molecular level, MOTS-c regulates metabolism by inhibiting the folate/methionine cycle in the nucleus. It binds to nuclear factors, reducing de novo purine biosynthesis, which leads to accumulation of 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR). AICAR is a potent activator of AMP-activated protein kinase (AMPK), mimicking energy stress and triggering catabolic pathways.
- Glycolysis Enhancement and AICAR Buildup: MOTS-c promotes glycolysis by shifting cellular reliance from oxidative phosphorylation (OXPHOS) to glycolytic flux under stress. This is achieved via AICAR-mediated AMPK activation, which phosphorylates targets like ACC (acetyl-CoA carboxylase), inhibiting fatty acid synthesis and favoring glucose uptake.
Recent studies (e.g., 2025 Nature article) confirm MOTS-c's role in pancreatic islets, where it boosts glycolytic enzymes like PFK1, preventing senescence.
- NAD+ Improvement and AMPK Synergy: MOTS-c elevates NAD+ levels by enhancing NAD+ salvage pathways and mitochondrial biogenesis via PGC-1α upregulation. Although AMPK activation typically depletes NAD+ in acute states, MOTS-c's chronic effects parallel NAD+ boosting (e.g., via SIRT1 activation), resolving the apparent paradox. This dual action supports mitochondrial repair and energy efficiency, as seen in 2025 NIH studies
showing restored OXPHOS and reduced ATP hydrolysis in damaged mitochondria.
- p53 Upregulation and NF-κB Downregulation: MOTS-c translocates to the nucleus, interacting with transcription factors to increase p53 expression, promoting DNA repair and apoptosis in stressed cells. Conversely, it suppresses NF-κB signaling, reducing pro-inflammatory cytokines like TNF-α and CRP. This anti-inflammatory profile is key for metabolic health, without elevating homocysteine or other markers, despite increased methylation (via methionine cycle modulation).
- Mitochondrial Damage Repair: MOTS-c improves mitochondrial function by increasing ROS in a controlled manner ( hormesis), enhancing OXPHOS capacity, and mitigating damage from aging or diabetes. 2025 Springer studies on diabetic cardiomyopathy show MOTS-c restores membrane potential and biogenesis, acting as a mitohormetic agent.
Metabolic and Physiological Benefits
MOTS-c's MoA extends to systemic effects, positioning it as a therapeutic for obesity, insulin resistance, and muscle health.
- Obesity Prevention and Body Recomposition: By activating AMPK, MOTS-c inhibits lipogenesis and promotes fat oxidation, preventing weight gain and liver fat accumulation (2025 Taylor & Francis study). It aids body recomposition by enhancing lean mass through myostatin inhibition, reducing muscle atrophy signals. This is particularly beneficial for age-related sarcopenia, where MOTS-c mimics exercise-induced muscle adaptations.
- Insulin Resistance Improvement: MOTS-c enhances insulin sensitivity via GLUT4 translocation and IRS-1 phosphorylation, countering resistance in type 2 diabetes models. In 2025 Nature research, it protected pancreatic islets in nonobese diabetic mice, improving glucose tolerance.
- Exercise Mimetic Properties: As an "exercise in a pill," MOTS-c replicates endurance training effects by boosting AMPK and PGC-1α, increasing mitochondrial density and aerobic capacity. 2025-2026 studies link exercise intensity to circulating MOTS-c levels, correlating with metabolic improvements.
- Methylation Effects Without Inflammatory Drawbacks: MOTS-c increases global DNA methylation by altering one-carbon metabolism, supporting epigenetic stability. However, it does not elevate inflammatory markers (CRP,TNF-α) or homocysteine, avoiding risks associated with hypermethylation therapies.
Similarities to Humanin and Applications in Neurodegeneration
MOTS-c exhibits Humanin-like effects, including neuroprotection and anti-apoptotic actions, but with a distinct structure (no shared sequence motifs) and administration routes (e.g., injectable vs. oral potential). In neurodegenerative diseases, MOTS-c modulates AMPK in neurons, reducing amyloid aggregation and tau phosphorylation. 2025 studies suggest applications in Alzheimer's, where it preserves synaptic function and mitochondrial integrity, differing from Humanin's IGFBP-3 binding.
Research setting HED:
- mitochondrial health, longevity, cardiac health, insulin sensitivity, morning 10mg sQ/ three times/week, 8 weeks, 4 weeks pause.
- kidney trials: morning 1mg/day sQ 12 weeks
- Weight-loss supporting research: 5mg/day in the morning, five days per week, for 20 days/month, for a 6-month period.
- loading dose approach trial protocol: 5mg/week for 6 weeks, followed by a 6-week break, then 5mg/week for 6 weeks. Maintenance phase: 5mg/month.
- adjunct supplementation: Co-administer B vitamins (e.g., B6, B12) and folic acid to mitigate folate cycle inhibition, preventing deficiencies and supporting methylation balance.
Related research context
To explore how mitochondrial efficiency and metabolic signaling intersect with muscle performance and recovery research, see:
→ Muscle Growth & Regeneration: Research Perspectives
Product Description:
- Chemical Formula : C101H152N28O22S2
- Synonyms : Mitochondria-derived peptide, mots-c, EX-A626, Met-Arg-Trp-Gln-Glu-Met-Gly-Tyr-Ile-Phe-Tyr-Pro-Arg-Lys-Leu-Arg
- Molar Mass : 2174.6 g/mol
- CAS Number : 1627580-64-6
- PubChem : 146675088
- Total Amount of the Active Ingredient : 20 mg (1 vial)
Source: PubChem
Product Usage
This item is supplied for research purposes only.
Peptide Storage
All information provided by PRG is for educational and informational purposes only.
Best Practices for Storing Peptides
To maintain the reliability of laboratory results, correct peptide storage is essential. Proper storage conditions help preserve peptide stability for years while protecting against contamination, oxidation, and breakdown. Although certain peptides are more sensitive than others, following these best practices will greatly extend their shelf life and structural integrity.
- Short-Term Storage (days to months): Keep peptides cool and protected from light. Temperatures below 4 °C (39 °F) are generally suitable. Lyophilized peptides often remain stable at room temperature for several weeks, but refrigeration is still preferred if use is not immediate.
- Long-Term Storage (months to years): Store peptides at –80 °C (–112 °F) for maximum stability. Avoid frost-free freezers, as defrost cycles can cause damaging temperature fluctuations.
- Minimize Freeze–Thaw Cycles: Repeated freezing and thawing accelerates degradation. Instead, divide peptides into aliquots before freezing.
Preventing Oxidation & Moisture Damage
Peptides can be compromised by exposure to moisture and air—especially immediately after removal from a freezer.
- Let the vial warm to room temperature before opening to prevent condensation.
- Keep containers sealed as much as possible, and if possible, reseal under a dry, inert gas such as nitrogen or argon.
- Amino acids like cysteine (C), methionine (M), and tryptophan (W) are particularly sensitive to oxidation.
Storing Peptides in Solution
Peptides in solution have a much shorter lifespan compared to lyophilized form and are prone to bacterial degradation.
- If storage in solution is unavoidable, use sterile buffers at pH 5–6.
- Prepare single-use aliquots to avoid repeated freeze–thaw cycles.
- Most peptide solutions are stable for up to 30 days at 4 °C (39 °F), but sensitive sequences should remain frozen when not in use.
Containers for Peptide Storage
Select containers that are clean, intact, chemically resistant, and appropriately sized for the sample.
- Glass vials: offer clarity, durability, and chemical resistance.
- Plastic vials: polystyrene (clear but less resistant) or polypropylene (translucent but chemically resistant).
- Peptides shipped in plastic vials may be transferred to glass for long-term storage if desired.
Regenesis Peptide Storage Quick Tips
- Keep peptides in a cold, dry, dark environment
- Avoid repeated freeze–thaw cycles
- Minimize exposure to air
- Protect from light
- Avoid storing in solution long term
- Aliquot peptides to match experimental needs